Objective To investigate the potential effects of rosuvastatin on white matter lesion and spatial memo?ry function in chronic hypertensive rats. Methods Fourty-nine male Sprague-Dawley rats were randomly divided into sham-operation group, vehicle-treated group, and rosuvastatin-treated group (10 mg/kg).A model of stroke-prone reno?vascular hypertensive rat (RHRSP) was induced by using the two-kidney two clip method in the vehicle-treated group and the rosuvastatin-treated group. Blood pressure was monitored regularly. Morris water maze experiment was conduct?ed to assess spatial memory function. Luxol fast blue stanning was used to examine the degree of leukoaraiosis. Immuno?fluorescence and electron microscopy was used to detectβ-amyloid deposits. TUNEL staining was used to assess apopto?sis. Results The blood pressure of RHRSP increased progressively after operation.Blood pressure was significantly high?er in RHRSP than in sham-operation group (P<0.01). The escape latencies of the rosuvastatin-treated group were mark?edly shorter in RHRSP than in sham-operation group (P<0.01). The numbers of crossing hidden platform in the 3 groups of rats were 4.55±1.23, 1.00±0.80 and 3.79±0.95 times. There were significantly differences in numbers of crossing hid? den platform among three groups (P<0.01). Luxol fast blue stanning showed that the grading scores for WML were lower in the rosuvastatin-treated than in the vehicle-treated group (P<0.01). Rosuvastatin significantly decreased the burden of Aβdeposits(17.47±3.59 vs. 4.42±1.57,P<0.01)and the TUNEL+cells(37.84±4.73 vs. 14.42±2.43,P<0.01)in the fron?tal cortex when compared with the vehicle-treated group. Conclusions Rosuvastatin may ameliorate spatial memory func?tion through attenuation of white matter lesion, Aβdeposits and apoptosis .

Aim To explore the apoptotic effect of mimics of manganese superoxide dismutase(MnSODm)on human leukemia cell line K562 in vitro and the possible molecular mechanisms.Methods Human leukemia K562 cells were used as the target cells.The cell proliferating activity was examined by a MTT colorimetric assay,and the apoptosis of K562 cells was assessed with FITC-Annexin V and propidium iodide(PI)double staining and morphological changes.The expressions of bcl-2 and bax mRNA were detected by reverse transcription polymerase chain reaction(RT-PCR),and flow cytometry(FCM)was employed to measure the expressions of Bcl-2 and Bax protein,mitochondrial inner membrane potential(??m),Cytochrome C(Cyt C)release and Caspase-3 activity.Results The proliferation of K562 cells was obviously inhibited by 0.5~10 mg?L-1 MnSODm(P

Aim To investigate the role of autophagy and its mechanism in Raji cell death induced by arse-nic trioxide. Methods Transmission electron micros-copy ( SEM) and MDC fluorescence staining were used to observe autophagy. MTT colorimetry was employed to assay the cellular proliferating activity. Cell apopto-sis and cell cycle analysis were performed using FITC-Annexin-V/PI double staining and flow cytometry ( FCM) . The expressions of LC3 and the conversion of LC3-I to LC3-II were measured by western bloting. The expression of bcl-2 mRNA and p53 mRNA were detected by reverse transcription-polymerase chain re-action ( RT-PCR ) . Results Arsenic trioxide could obviously inhibit the proliferation of Raji cells, arrest the cells at G2/M phase and induce apoptosis. Mean-while, arsenic trioxide markedly inhibited the expres-sion of bcl-2 mRNA and enhanced the expression of p53 mRNA in Raji cells. Arsenic trioxide also induced autophagy synchronously which paralleled with the in-duction of apoptosis in Raji cells, and 3-MA, an auto-phagy inhibitor, was able to reverse the arsenic triox-ide-activated autophagic activity, up-regulate bcl-2, down-regulated p53 expression and suppress the lethal effect of arsenic trioxide on Raji cells to reduce their sensitivity to arsenic trioxide. In contrast, the Rapamy-cin, an autophagy inducer, possessed the completely opposite effects on Raji cells compared with 3-MA. Conclusions The apoptosis and autophagic cell death are coexistent in arsenic trioxide-triggered death of Raji lymphoma cells, and Bcl-2 and p53 may play a key regulating role in this process.